Vascular smooth muscle cell migration, proliferation, and matrix synthesis within the intima of medium-sized and large vessels is thought to play a major role in atherosclerosis development in adult human subjects. In the embryo, these vascular cells have a complex origin, with the first smooth muscle cells surrounding endothelial tubes being derived from trans-differentiated endothelium during nascent vascular and cardiac valve development. Several growth factors have been implicated in embryonic smooth muscle cell differentiation, including transforming growth factors β1, β3, and platelet-derived growth factor BB (PDGF-BB).
Understanding the phenotype of any circulating smooth muscle progenitor cell may have implications for development of therapies to modulate homing of these cells to the vessel wall. Intrinsic to this latter understanding may be the identification of specific surface adhesion molecules, such as integrins, which are known to be important in homing of blood-borne progenitor cells to specific sites in vivo.